Salmonella enterica serovar typhi plasmid pR ST98 enhances intracellular bacterial growth and S. typhi-induced macrophage cell death by suppressing autophagy

He, Peiyan; Wu, Shuyan; Chu, Yuanyuan; Yang, Yan‐Ru; Li, Yuanyuan; Huang, Rui

doi:10.1590/s1413-86702012000300008

Cited by 7 publications

(5 citation statements)

References 13 publications

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“…pR (ST98) has a molecular weight of 98.6 × 10 6 Da (about 159 kb), and was first identified and reported by Huang et al (2005). Subsequent studies in their laboratory have shown that mutant Salmonella, harboring a pR (ST98) plasmid deletion, inhibited autophagy in infected macrophages (He et al, 2012;Chu et al, 2014;Wu et al, 2014) and mouse embryonic fibroblasts (Lv et al, 2012), while enhancing Salmonella proliferation within cells and consequently promoting cell death. These results demonstrate that the pR (ST98) plasmid enables Salmonella to escape autophagy.…”

Section: The Escape Mechanism Employed By Salmonella To Evade Host Cementioning

confidence: 99%

Salmonella Interacts With Autophagy to Offense or Defense

Shen

Zhang

et al. 2020

Front. Microbiol.

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Autophagy is an important component of the innate immune system in mammals. Low levels of basic autophagy are sustained in normal cells, to help with the clearance of aging organelles and misfolded proteins, thus maintaining their structural and functional stability. However, when cells are faced with challenges, such as starvation or pathogenic infection, their level of autophagy increases significantly. Salmonella is a facultative intracellular pathogen, which imposes an economic burden on the poultry farming industry and human public health. Previous studies have shown that Salmonella can induce the autophagy of cells following invasion, which to a certain extent helps to protect the cells from bacterial colonization. This review summarizes the latest research in the field of Salmonella-induced autophagy, including: (i) the autophagy induction and escape mechanisms employed by Salmonella during the infection of host cells; (ii) the effect of autophagy on intracellular Salmonella; (iii) the important autophagy adaptors that recognize intracellular Salmonella in host cells; and (iv) the effect of autophagy-modulating drugs on Salmonella infection.

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Section: The Escape Mechanism Employed By Salmonella To Evade Host Cementioning

confidence: 99%

Salmonella Interacts With Autophagy to Offense or Defense

Shen

Zhang

et al. 2020

Front. Microbiol.

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“…SseK3 is essential for cellular Salmonella infection, and plays a pivotal role in the natural host immune process [15,17]. Several secretory proteins of S. Typhimurium contribute to the considerable stress observed during apoptosis [24,25,27,28]. There were several studies about the function of SseK3.…”

Section: Discussionmentioning

confidence: 99%

Salmonella enterica serovar Typhimurium sseK3 induces apoptosis and enhances glycolysis in macrophages

Chen

Zhang

et al. 2020

BMC Microbiol

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Background: Salmonella enterica serovar Typhimurium (S. Typhimurium) is an important infectious disease pathogen that can survive and replicate in macrophages. Glycolysis is essential for immune responses against S. Typhimurium infection in macrophages, and is also associated with apoptosis. S. Typhimurium secreted effector K3 (SseK3) was recently identified as a novel translated and secreted protein. However, there is no study about the role of sseK3 in the relationship between apoptosis and glycolysis in cells infected with S. Typhimurium. It is unclear whether this protein exerts a significant role in the progress of apoptosis and glycolysis in S. Typhimurium-infected macrophages. Results: Macrophages were infected with S. Typhimurium SL1344 wild-type (WT), ΔsseK3 mutant or sseK3complemented strain, and the effects of sseK3 on apoptosis and glycolysis were determined. The adherence and invasion in the ΔsseK3 mutant group were similar to that in the WT and sseK3-complemented groups, indicating that SseK3 was not essential for the adherence and invasion of S. Typhimurium in macrophages. However, the percentage of apoptosis in the ΔsseK3 mutant group was much lower than that in the WT and sseK3complemented groups. Caspase-3, caspase-8, and caspase-9 enzyme activity in the ΔsseK3 mutant group were significantly lower than in the WT group and sseK3-complemented groups, indicating that sseK3 could improve the caspase-3, caspase-8, and caspase-9 enzyme activity. We also found that there were no significant differences in pyruvic acid levels between the three groups, but the lactic acid level in the ΔsseK3 mutant group was much lower than that in the WT and sseK3-complemented groups. The ATP levels in the ΔsseK3 mutant group were remarkably higher than those in the WT and sseK3-complemented groups. These indicated that the sseK3 enhanced the level of glycolysis in macrophages infected by S. Typhimurium. Conclusions: S. Typhimurium sseK3 is likely involved in promoting macrophage apoptosis and modulating glycolysis in macrophages. Our results could improve our understanding of the relationship between apoptosis and glycolysis in macrophages induced by S. Typhimurium sseK3.

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“…SseK3 is essential for cellular Salmonella infection, and plays a pivotal role in the natural host immune process [16,18]. Several secretory proteins of S. Typhimurium contribute to the considerable stress observed during apoptosis [25,26,28,29]. There were several studies about the function of SseK3.…”

Section: Discussionmentioning

confidence: 99%

Salmonella enterica serovar Typhimurium sseK3 induces apoptosis and enhances glycolysis in macrophages

Chen

Zhang³

et al. 2020

Preprint

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Background: Salmonella enterica serovar Typhimurium (S. Typhimurium) is an important infectious disease pathogen that can survive and replicate in macrophages. Glycolysis is essential for immune responses against S. Typhimurium infection in macrophages, and is also associated with apoptosis. S. Typhimurium secreted effector K3 (SseK3) was recently identified as a novel translated and secreted protein. However, there is no study about the role of sseK3 in the relationship between apoptosis and glycolysis in cells infected with S. Typhimurium. It is unclear whether this protein exerts a significant role in the progress of apoptosis and glycolysis in S. Typhimurium-infected macrophages.Results: Macrophages were infected with S. Typhimurium SL1344 wild-type (WT), ΔsseK3 mutant or sseK3-complemented strain, and the effects of sseK3 on apoptosis and glycolysis were determined. The adherence and invasion in the ΔsseK3 mutant group were similar to that in the WT and sseK3-complemented groups, indicating that SseK3 was not essential for the adherence and invasion of S. Typhimurium in macrophages. However, the percentage of apoptosis in the ΔsseK3 mutant group was much lower than that in the WT and sseK3-complemented groups. Caspase-3, caspase-8, and caspase-9 enzyme activity in the ΔsseK3 mutant group were significantly lower than in the WT group and sseK3-complemented groups, indicating that sseK3 could improve the caspase-3, caspase-8, and caspase-9 enzyme activity. We also found that there were no significant differences in pyruvic acid levels between the three groups, but the lactic acid level in the ΔsseK3 mutant group was much lower than that in the WT and sseK3-complemented groups. The ATP levels in the ΔsseK3 mutant group were remarkably higher than those in the WT and sseK3-complemented groups. These indicated that the sseK3 enhanced the level of glycolysis in macrophages infected by S. Typhimurium.Conclusions: S. Typhimurium sseK3 is likely involved in promoting macrophage apoptosis and modulating glycolysis in macrophages. Our results could improve our understanding of the relationship between apoptosis and glycolysis in macrophages induced by S. Typhimurium sseK3.

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Salmonella enterica serovar typhi plasmid pR ST98 enhances intracellular bacterial growth and S. typhi-induced macrophage cell death by suppressing autophagy

Abstract: Plasmid pR ST98 enhances intracellular bacterial growth and S. typhi-induced macrophage cell death by suppressing autophagy.

Cited by 7 publications

References 13 publications

Salmonella Interacts With Autophagy to Offense or Defense

Salmonella Interacts With Autophagy to Offense or Defense

Salmonella enterica serovar Typhimurium sseK3 induces apoptosis and enhances glycolysis in macrophages

Salmonella enterica serovar Typhimurium sseK3 induces apoptosis and enhances glycolysis in macrophages

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